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Related Experiment Video

Updated: Aug 6, 2025

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Vascular-Parenchymal Cross-Talk Promotes Lung Fibrosis through BMPR2 Signaling.

Toyoshi Yanagihara1,2, Kazuya Tsubouchi1,2, Quan Zhou1

  • 1Firestone Institute for Respiratory Health, Research Institute at St. Joseph's Healthcare, and.

American Journal of Respiratory and Critical Care Medicine
|March 14, 2023
PubMed
Summary

Idiopathic pulmonary fibrosis (IPF) with pulmonary hypertension (PH) involves vascular remodeling and impaired BMPR2 signaling. Tacrolimus shows promise in treating IPF and PH, with genetic factors also playing a role.

Keywords:
BMPR2idiopathic pulmonary fibrosispulmonary hypertensiontacrolimusvascular remodeling

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Area of Science:

  • Pulmonary Medicine
  • Vascular Biology
  • Genetics

Background:

  • Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung scarring disease.
  • Pulmonary vascular remodeling and pulmonary hypertension (PH) significantly worsen IPF prognosis.
  • Understanding the mechanisms of vascular changes in IPF is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the pathogenesis of vascular remodeling in fibrotic lungs.
  • To determine the contribution of vascular remodeling to fibrosis progression.
  • To explore the role of BMPR2 signaling in IPF-associated PH.

Main Methods:

  • Utilized a rodent model of lung fibrosis with PH induced by TGF-β1 overexpression.
  • Analyzed patient samples using immunostaining, gene expression, and whole-exome sequencing.
  • Employed co-culture systems to study cell interactions between fibroblasts, endothelial cells (ECs), and vascular smooth muscle cells (VSMCs).

Main Results:

  • Fibrotic lungs showed reduced ECs and activated VSMCs, with impaired BMPR2 signaling in both cell types.
  • Fibroblast interactions with fibrotic ECs/VSMCs promoted fibrotic phenotypes.
  • Tacrolimus treatment attenuated fibrosis and PH in rodent models by activating BMPR2 signaling.
  • Rare BMPR2 mutations, including a novel dysfunctional variant (p.Q721R), were identified in IPF patients with PH.

Conclusions:

  • Endothelial dysfunction and vascular remodeling in IPF-related PH exacerbate fibrogenesis via impaired BMPR2 signaling.
  • Tacrolimus demonstrates potential as a therapeutic agent for advanced IPF and associated PH.
  • Genetic abnormalities, particularly in BMPR2, may predispose individuals to developing PH in advanced IPF.